Key result
Chondroitin C inhibits platelet spreadability by ~42% whereas heparin increases it.
Why the study?
Do acid glycosaminoglycans influence platelet spreadability and aggregation in vitro?
Do acid glycosaminoglycans influence platelet spreadability and aggregation in vitro?
Acid glycosaminoglycans present in the vascular endothelium, particularly chondroitin C, inhibit platelet spreading and adhesion, suggesting a regulatory role in vascular endothelium-platelet interactions.
Answers are grounded in this paper and cite their sources.
Supports endothelial chondroitin C as a platelet regulator in vitro; leaves open in vivo antithrombotic relevance.
The influence of various acid glycosaminoglycans on the platelet spreadability (PSA) was studied, along with the platelet aggregation test (PAT) and ADP aggregation test.Acid glycosaminoglycans; chondroitin-6-sulfate (chondroitin A) dermatan sulfate (chondroitin B) and chondroitin-4-sulfate (chondroitin C) present in vascular endothelirium and heparin, amyropectin sulfate, amylose sulfate, glycogen sulfate and glycogen were added to PRP at the concentration of 0.0025mg/ml after 15 minutes, the number of platelets adhering to the plastic plate was counted to ovserve the spreading of platelet. PAT was conducted by Breddin I method and ADP aggregation induced by 10-5M. ADP was measured in the same sample.Addition of chondroitin C resulted in a marked decrease of the plastic plate adhesion on the plastic plate with disturbance of platelet spreading, indicating a definite inhibition of PSA. PAT was mildly inhibited. Chondroitin A and B mildly inhibited PSA but the responses of PAT were variable. Heparin definitely augmented both PAT and PSA with an increase of platelet adhesion on plastic plate. Amylose sulfate and amylopectin sulfate failed to influence the spreading definitly. While glycogen sulfate augmented PAT and PSA, glycogen exerted no such action. No difinite change occurred in aggregation in response to any of these substances tested.Three of the acid glycosaminoglycans present in the vascular endothelium inhibited platelet spreading and interfered with the platelet adhesion to the plastic plate. Especially chondroitin C most abundantly found with in the endothelium showed a marked inhibitly effect. Heparin, on the contrary, interestingly augmented platelet adhesion at 0.0025mg/ml. Other acid glycosaminoglycans showed no inhibitory action on platelet adhesion. These observation provably suggest the relationship between acid glycosaminoglycans in the vascular endotherium and platelets.
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TSUKAHARA et al. (1980) studied Healthy subjects (in vitro). Acid glycosaminoglycans (e.g., chondroitin C, heparin) vs. Control (untreated PRP) was evaluated on Platelet spreadability (PSA) relative to control (p=<0.01). Chondroitin C significantly inhibited platelet spreadability to 57.7% of control (p<0.01), whereas heparin at 0.0025 mg/ml augmented it to 164.1% (p<0.01).
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